The threshold for diagnosing impaired fasting glucose: a position statement by the European Diabetes Epidemiology Group

Forouhi, Nita G.; Balkau, Beverley; Borch‐Johnsen, Knut; Dekker, J.; Glümer, Charlotte; Qiao, Qing; Spijkerman, Annemieke M.W.; Stolk, Ronald P.; Tabac, Alliance Contre le; Wareham, Nick; Edeg,

doi:10.1007/s00125-006-0189-4

Cited by 114 publications

(66 citation statements)

References 33 publications

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“…The DECODE (Diabetes Epidemiology: Collaborative analysis of Diagnostic criteria in Europe) study group also found that the 7-year risk of coronary heart disease was lower in women with a fasting glucose value between 5.6 and 6.0 mmol/l compared with women with NFG (20). Because of such findings, the lower cutoff of the 2003 ADA criteria for IFG has been questioned (21,22). This reported J-shape and the results of the present study are strong reasons to reconsider the recommendation to lower the IFG cutoff to 5.6 mmol/l.…”

Section: Consequences Of Lowering the Ifg Cutoff For Cvd Riskmentioning

confidence: 62%

High Risk of Cardiovascular Mortality in Individuals With Impaired Fasting Glucose Is Explained by Conversion to Diabetes

et al. 2007

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OBJECTIVE—To optimize identification of future diabetic patients, the American Diabetes Association (ADA) introduced criteria for impaired fasting glucose (IFG) in 1997 (IFG 6.1 mmol/l [IFG6.1]) and lowered the threshold from 6.1 to 5.6 mmol/l (IFG5.6) in 2003. Our aim was to assess the consequences of lowering the IFG cutoff on the risk of cardiovascular disease (CVD) mortality and to evaluate whether this risk is explained by a conversion to type 2 diabetes within 6.4 years. RESEARCH DESIGN AND METHODS—In a population-based cohort, the Hoorn Study, plasma glucose was determined in 1989 and 1996 (n = 1,428). Subjects were classified in 1989 according to 1997 and 2003 ADA criteria. Subjects with IFG in 1989 were further classified according to diabetes status in 1996. Hazard ratios for CVD mortality (n = 81) in the period 1996–2005 were adjusted for age and sex. RESULTS—Subjects with IFG6.1, but not IFG5.6, had a significantly higher CVD mortality risk than normal fasting glucose (NFG) subjects. Subjects who converted from IFG to diabetes (IFG6.1: 42%; IFG5.6: 21%) had a more than twofold risk of CVD mortality (IFG6.1: 2.47 [1.17–5.19]; IFG5.6: 2.14 [1.12–4.10]) than subjects with NFG. IFG subjects who did not develop diabetes did not have significantly higher CVD mortality risks (IFG6.1: 1.50 [0.72–3.15]; IFG5.6: 1.15 [0.69–1.93]). CONCLUSIONS—The lower cutoff for IFG (ADA 2003 criteria) results in a category of IFG that no longer represents a high-risk state of CVD. Furthermore, only subjects who convert from IFG to diabetes have a high risk of CVD mortality.

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Section: Consequences Of Lowering the Ifg Cutoff For Cvd Riskmentioning

confidence: 62%

High Risk of Cardiovascular Mortality in Individuals With Impaired Fasting Glucose Is Explained by Conversion to Diabetes

et al. 2007

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“…We obtained venous plasma samples at 0, 30, 60, 90 and 120 min for determination of plasma glucose and insulin. Glucose tolerance was evaluated based on OGTT as follows: NGT (fasting glucose <5.6 mmol/l and 2 h glucose <7.8 mmol/l); isolated IFG (fasting glucose 5.6-6.9 mmol/l and 2 h glucose <7.8 mmol/l); isolated IGT (fasting glucose <5.6 mmol/l and 2 h glucose 7.8-11.0 mmol/l); and IFG+IGT (fasting glucose 5.6-6.9 mmol/l and 2 h glucose 7.8-11.0 mmol/l) [30,31].…”

Section: Methodsmentioning

confidence: 99%

The impact of liver fat vs visceral fat in determining categories of prediabetes

et al. 2010

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Aims/hypothesis Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are risk factors for type 2 diabetes and cardiovascular disease; however, their impact on these endpoints differs. Because liver fat and visceral fat are important determinants of glucose and lipid metabolism, we investigated whether these fat compartments and their humoral products, the adipokine adiponectin and the hepatokine fetuin-A, differ in their impact on the glucose categories. Methods In 330 individuals at risk of type 2 diabetes, glucose tolerance status was determined by a 2 h 75 g OGTT. Total-body and visceral fat were precisely quantified by magnetic resonance (MR) tomography and liver fat by 1 H-MR spectroscopy. Results A total of 210 individuals had normal glucose tolerance (NGT), 41 isolated IFG, 43 isolated IGT and 36 IFG+IGT. Total-body fat was not different (p=0.51), although a small but continuous increase in visceral fat was found among the categories after adjustment for age and sex (NGT: 3.07±0.10 kg; IFG: 3.11±0.21 kg; IGT: 3.61 ± 0.21 kg; IFG +IGT: 3.84±0.23 kg [SEs], p=0.03). A larger difference was found for liver fat (NGT: 4.73±0.42%; IFG: 5.86±0.92%; IGT: 8.65±0.92%; IFG+IGT: 11.11±1.01%, p<0.0001). The differences among the categories were small for adiponectin (p=0.14), but larger for fetuin-A (p=0.015). Among fat compartments, liver fat (p<0.0001) and among circulating variables fetuin-A (p=0.016) were the strongest determinants of the categories. Conclusions/interpretation Liver fat, more than visceral fat, strongly increases when glycaemia and glucose tolerance move from NGT to isolated IFG, isolated IGT and IFG+IGT. Because liver-derived circulating fetuin-A determines, although weakly, prediabetes categories, it is worth searching for hepatokines more strongly predicting prediabetes.

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“…This change has been contentious and has not been accepted by all organizations (19,38 ). The rationale is based on data that individuals with FPG values between 5.6 mmol/L (100 mg/dL) and 6.05 mmol/L (109 mg/dL) are at increased risk for developing type 2 diabetes (39,40 ).…”

Section: B the Nacb Recommends Adoptionmentioning

confidence: 99%

Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus

et al. 2011

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BACKGROUND Multiple laboratory tests are used to diagnose and manage patients with diabetes mellitus. The quality of the scientific evidence supporting the use of these tests varies substantially. APPROACH An expert committee compiled evidence-based recommendations for the use of laboratory testing for patients with diabetes. A new system was developed to grade the overall quality of the evidence and the strength of the recommendations. Draft guidelines were posted on the Internet and presented at the 2007 Arnold O. Beckman Conference. The document was modified in response to oral and written comments, and a revised draft was posted in 2010 and again modified in response to written comments. The National Academy of Clinical Biochemistry and the Evidence Based Laboratory Medicine Committee of the AACC jointly reviewed the guidelines, which were accepted after revisions by the Professional Practice Committee and subsequently approved by the Executive Committee of the American Diabetes Association. CONTENT In addition to long-standing criteria based on measurement of plasma glucose, diabetes can be diagnosed by demonstrating increased blood hemoglobin A1c (Hb A1c) concentrations. Monitoring of glycemic control is performed by self-monitoring of plasma or blood glucose with meters and by laboratory analysis of Hb A1c. The potential roles of noninvasive glucose monitoring, genetic testing, and measurement of autoantibodies, urine albumin, insulin, proinsulin, C-peptide, and other analytes are addressed. SUMMARY The guidelines provide specific recommendations that are based on published data or derived from expert consensus. Several analytes have minimal clinical value at present, and their measurement is not recommended.

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The threshold for diagnosing impaired fasting glucose: a position statement by the European Diabetes Epidemiology Group

Abstract: The category of IFG was introduced in the late 1990s to denote a state of non-diabetic hyperglycaemia defined by a fasting plasma glucose (FPG) concentration between 6.1 and 6.9 mmol/l. In

Cited by 114 publications

References 33 publications

High Risk of Cardiovascular Mortality in Individuals With Impaired Fasting Glucose Is Explained by Conversion to Diabetes

High Risk of Cardiovascular Mortality in Individuals With Impaired Fasting Glucose Is Explained by Conversion to Diabetes

The impact of liver fat vs visceral fat in determining categories of prediabetes

Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus

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